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RhoG, a member of the Rho family of GTPases, has been implicated as a regulator of the actin cytoskeleton. In this study, we show a novel function for the small GTPase RhoG on the regulation of the interferon-gamma promoter and nuclear factor of activated T cells (NFAT) gene transcription in lymphocytes. Optimal function of RhoG for the expression of these genes requires a calcium signal, normally provided by the antigen receptor. In addition, RhoG potentiation of NFAT requires the indirect activity of Rac and Cdc42; however, pathways distinct from those activated by Rac and Cdc42 mediate RhoG activation of NFAT-dependent transcription. Using effector domain mutants of RhoG we found that its ability to potentiate NFAT-dependent transcription correlates with its capacity to increase actin polymerization, supporting the suggestion that NFAT-dependent transcription is an actin-dependent process. RhoG also promotes T-cell spreading on fibronectin, a property that is independent of its ability to enhance NFAT-dependent transcription. Hence, these results implicate RhoG in leukocyte trafficking and the control of gene expression induced in response to antigen encounter.

Original publication

DOI

10.1038/sj.onc.1206116

Type

Journal article

Journal

Oncogene

Publication Date

23/01/2003

Volume

22

Pages

330 - 342

Keywords

Actins, B-Lymphocytes, Calcium, Cell Cycle Proteins, Cells, Cultured, Cytoskeleton, DNA-Binding Proteins, Fibronectins, GTP Phosphohydrolases, Gene Expression Regulation, Humans, Interferon-gamma, Jurkat Cells, Leukocytes, Lymphocytes, Mutation, NFATC Transcription Factors, Nuclear Proteins, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-vav, Signal Transduction, T-Lymphocytes, Transcription Factors, Transcription, Genetic, cdc42 GTP-Binding Protein, rac1 GTP-Binding Protein, rho GTP-Binding Proteins